The goal of this project is to determine the function of the rex gene of phage lambda. This gene is notable in two respects: 1) It is expressed by the prophage of an E. coli (lambda) lysogen, and 2) it is dispensable and has no known function. Recently I have found that rex aids in maintaining lysogeny and in timing host cell lysis. It also modifies the host's machinery for regulating cell division. Significantly, most rex effects are visible only in mutant hosts having altered energy metabolism, colicin sensitivity, cyclic AMP levels, or DNA metabolism. Rex diminishes the effects of these mutations on the viral growth cycle. We propose that when a lambda phage infects E. coli, it takes over certain regulatory systems of that cell to coordinate its own replication cycle. The role of rex is to correct strain-to-strain variations in these host control systems. Thus it expands the spectrum of strains and growth conditions in which lambda phage grows in a highly stereotyped way. Rex is reminiscent of the transforming proteins of oncogenic animal viruses and may be their functional equivalent. These also are viral proteins which redirect major regulatory systems of the host during latent viral infection. One objective of our study is to develop a bacteriological model for posing two outstanding questions about cancer: Why do oncogenic viruses have genes for transforming proteins? and How do these genes cause cell transformation? We propose to: 1) isolate and characterize a variety of lambda rex mutants; 2) catalogue the bacterial mutations that affect rex activity and describe their interactions with rex; 3) characterize the effect of rex on cell division, colicin tolerance, and energy metabolism of the lysogenic host; and 4) determine the relationships of cell division and rex to host cell lysis and of rex and colicin sensitivity to maintenance of lysogeny.